TRANS FATS: A MAJOR THREAT TO PUBLIC HEALTH
For centuries, lard was a household staple, including during the era between 1850 and 1946, when the U.S. had the best diet in the world. Shrovetide, the Anglo-Saxon name for Mardi gras, takes its name from the draining of animal fats from storage vatsand their consumption prior to Lent. However, during the '20s, the price of lard shot up abruptly. Vegetable oil is a readily available substitute, but it is a liquid at room temperature, while lard is a solid, and industrialists thought or told themselves that the consumer would not accept the liquid vegetable oil (e.g. Wesson®). Lard is a solid at room temperature because it is a saturated fat with no double or triple bonds in its hydrocarbon chains, while vegetable oil is polyunsaturated fat with double and triple bonds in its carbon chains (fig. 1). These unsaturated bonds raise its melting point, making it a liquid at room temperature. So when industrialists asked their chemists to transform the liquid vegetable oil into a solid that they thought was more marketable, they did so by passing hydrogen gas (H2) over it, a process called hydrogenization, which saturated out all the double and triple bonds. And so Crisco® was born.
But there was one slight problem, of which no one was aware until the better part of a century later. Animal fats are all cis fats, while synthetically hydrogenated fats are trans fats which do not exist in nature. Our lipid catabolic enzymes are adapted for cis fats, not trans fats. There is a constant turnover of cis fats in our bodies as we mobilize fat reserves for energy whenever hard times of any kind befall us. However, since our lipid catabolic enzymes are designed only for cis fats, trans fats merely accumulate in our bodies. They are not stored in our adipose tissue (body fat) because our lipid anabolic enzymes only make cis fats for storage. Rather, trans fats end up in our cellular membranes.
All cellular membranes consist of a lipid bilayer (fig. 2). Most people have noticed that oil (fat) and water do not mix. This is because water is polar, while hydrocarbon is not. Water is a bent, V-shaped molecule, with the oxygen in the middle and the 2 hydrogens at either end (fig. 3). The electrons in its molecular orbitals hang out around the oxygen because it is decisively a nonmetal, seeking two more electrons to complete its valence orbitals and leaving a positively-charged bald spot at each of the protons that are the two hydrogens. This is why water is polar. Other polar substances and charged ions and molecules mix well with water because all the opposite charges attract each other. However, hydrocarbon is nonpolar and has no electrostatic charges to share with water. This is why oil (the organic phase) floats above the aqueous phase, which is denser.
Each molecule of the lipid bilayer consists of a phosphate with 2 hydrocarbons attached. The phosphates are negatively charged ions, while the hydrocarbons are nonpolar fats. The positively charged sodium counterions are lurking about in the aqueous solution nearby the phosphates. The phosphates line both the exterior of the cell facing the aqueous lymphatic fluid and the inner surface of the cellular membrane facing the cytosol, which is also aqueous. In between the two layers of phosphates are the two layers of hydrocarbon, in their own nonpolar environment in the interior of the cellular membrane. Afloat in the membrane like icebergs are proteins which typically traverse the entire bilayer. The proteins are evolved so that all the polar or charged amino acid residues stick out on either end, where they are exposed either to the aqueous lymphatic fluid without or the cytosol within, while the nonpolar amino acid residues are tucked in the interior of the membrane amid the hydrocarbons.
In a healthy membrane, the phospholipids in the bilayer are not static but flow laterally past each other like people milling about in a large crowd. This fluidity allows the floating proteins to change conformation as needed to open and close ion channels and activate pumps, import and export substances, and respond to various intercellular transmitters and hormones. Animal fats can raise the melting point of the membrane, making it more rigid, but these are frequently turned over by lipid catabolic enzymes that are well-adapted to breaking them down, so they do not accumulate in the membrane. However, these enzymes are not adapted to breaking down trans fats, and consequently these synthetic fats accumulate in the membrane, inexorably raising its melting point and making it stiffer and stiffer. The proteins afloat are then no longer able to change conformation and perform their functions. Among these disabled proteins are the insulin receptors, which are no longer able to change conformation to import glucose and insulin into the cell. This is “type 2 diabetes.” Starved for glucose, the cell turns to fat catabolism to survive. With trillions of cells mobilizing fat(triglycerides) all at once for fuel, serum levels of these substances escalate to accommodate the demand. This is “metabolic disorder.”
This condition is so radically different from “type 1 diabetes” that it should be renamed to eliminate all the confusion it engenders. For most people, the term “diabetes” evokes images of defunct pancreatic beta islet endocrine cells, absent insulin, and replacement of this lost hormone by injection. However, in “type 2,” nothing can be further from the truth. The pancreatic endocrine function is perfectly fine, insulin is abundant, even excessive, and insulin injections are like pouring water on a drowning person. There are no circulatory sequelae from “type 2” because, unlike “type 1,” there are no defunct pancreatic alpha islet cells next door to the beta islet cells charged with manufacturing insulin because the pancreas is perfectly normal. Rather, the same stiff cellular membranes crippling insulin receptors also impinge on the ability of neurotransmitter receptors to function, significantly contributing to the epidemic of “depression,” “anxiety,” and “bipolar.” Of course, a major caveat is the inexorably escalating crises of family abuse, geopolitics, the environment, economics, gender, race and caste, education, media, and many other issues stemming from the brutal overclass campaign to achieve hegemony posing a clear and present threat to the physical survival of the biosphere. Under these circumstances, anyone who is not depressed, anxious, or both is morally dysfunctional. Not to even mention the certain causative role of general anesthesia in the epidemic of “depression” and other “mood disorders”!
If doctors were real scientists, they should know all this, but their “treatments” betray that they by and large do not. The aforementioned failure to rename the condition is a case in point. Rather than addressing the cellular membrane issue, many pills for “type 2 diabetes” merely block the liver from converting stored glycogen into glucose, which, of course, is harmful to the liver. Recall a major study in 2007 that had to be stopped because people taking more of such drugs were having more heart attacks than those with higher blood sugars taking fewer or no drugs. Back in 1969, a similar study also had to be stopped because patients taking these drugs were having more heart attacks than those who didn’t. Both studies were completely disregarded, which constitutes criminal negligence. Rezulin®, Avandia®, and now Januvia® are being implicated as causing heart attacks and/or other serious iatrogenic health problems.
So what is the treatment for poisoned cellular membranes? If trans fat is totally abolished from the diet, thenthat which is already in the membranes will just remain without additional intervention. The way to start forcing the trans fat out of the cellular membranes is by supplementation with omega-3 fatty acid(fish oil) at each meal. Implementation should be incremental, because blood sugar will drop with each administration of the supplement. One should start with one capsule a day in the morning, monitoring with a common glucometer. Once the body has adjusted to it, a second administration can be introduced in the evening, again using a glucometer to monitor blood sugar. Finally, the third dose is added at midday. This polyunsaturated fat will quickly start to enter the lipid bilayer, forcing out the trans fat by physical displacement. This will lower the melting point of the lipid bilayer, restoring its fluidity and freeing the embedded proteinaceous receptors to be able to change conformationonce again. The outflow of trans fats from the cellular membranes then forces the equilibrium of lipid catabolism to the right (towards products rather than reagents), forcing some of the trans fatinto the ill-fitting lipid catabolic enzymeswhich are evolved for cis fats. Because of the awkwardness of this forced poor fit, the process of catabolizing the trans fat takes years or decades. All biochemical treatments are long-term therapies and not quick fixes, and are cumulative.
Because biochemical treatments are so long-term and often take time to show a dramatic improvement, one diabetes drug, metformin (Glucophage®), can help tame blood sugars over the short term while trans fat is slowly being forced out of membranes, although it is stressful to the liver over the long run. Unlike so many others, it is not linked to heart disease or pancreatic damage. However, it should not be used as a weight loss drug, because the effect is often the opposite! This weight gain is also caused by other diabetes drugs, because artificially lowering blood sugar invariably and inescapably increases the appetite. Another drug that can help corral blood sugar without jeopardizing the heart or pancreas is glyburide. This substance can also help ease stress to the kidney inflicted by high blood pressure, having to process excessive amounts of nitrogenous waste from protein catabolism, or fromhaving to excrete excess sugar.
A trace element supplement that is helpful to both insulin-dependent “type 1” diabetics and victims of trans fat poisoning is chromium, because it is involved in common glucose catabolism. Insulin-dependent type 1 diabetics will need to monitor themselves closely with a glucometer when starting chromium and reduce their insulin dosage accordingly. Dosage of chromium supplements are in the microgram (g) range rather than the milligram (mg) range and should be taken once daily. Too much chromium, like many trace metals, can be toxic, but given the pathetic mineral-depleted state of the soil because of unsustainable agribusiness, only an accidental overdose of the supplement will create toxicity from chromium poisoning. I recommend using a jumbo pill minder for all supplements to help prevent an accidental OD.
Elsewhere on the Articles page is a medical news post about a poster presentation at the 2010 ENDO meeting acknowledging (read admitting) the benefit of antioxidant supplements to “type 2” patients (read victims of trans fat poisoning). A potent antioxidant that substantially increases insulin sensitivity which I have personal experience with is alpha-lipoic acid (ALA). Start out with 500 milligrams (mg), monitoring with a glucometer. If at this point, blood sugars are consistently running below 130mg/dL without drugs, than that dose will be sufficient. If they are consistently running over 150 mg/dL without drugs, then increase the dose of ALA to 1 gram (1000 mg), again monitoring with a glucometer. This is the highest dose recommended, which should be taken once a day.
Other very common antioxidants are vitamins C and E. Vitamin C (ascorbic acid) should be taken twice a day, approximately 12 hours apart, because the human body cannot store it (carnivorous animals such as cats actually have an ascorbic acid anabolic pathway that human beings do not have). 500 mg of ascorbic acid per dose should be the bare minimum for a noncancerous person. Vitamin E (alpha-L-tocopherol) can be taken once or twice daily as the body has limited capacity to store it. But the most important consideration regarding vitamin E is its stereochemistry. Unlike ascorbic acid, one carbon of tocopherol has a different group attached to it via each of its 4 bonds. Such an asymmetrical carbon is called chiral, and the different groups can be arranged about it in 2 distinctly different ways. Please see the lesson plan at the conclusion of my term paper found in the education block on the Articles page for a ball-and-stick exercise about chirality. The 2 different possible arrangements are called enantiomers, but all of their chemical properties remain identical. Unlike cis (same side) and trans (opposite side) chemical variants, which can be easily shown in simple Lewis diagrams (fig. 4), dextrorotary and levorotary enantiomers cannot be illustrated in two-dimensional Lewis diagrams, and can only be shown in 3 dimensions (the terms dextrorotary and levorotary refer to the fact that solutions of a pure enantiomer will rotate a beam of circularly polarized light passed through them either to the right or to the left, hence the abbreviations D and L for each enantiomer). Most biologically active enantiomers are levorotary, with dextrose (glucose) being an exception. The opposite enantiomer is invariably biologically inert because all enzymes are proteins which fold into a 3-dimensional tertiary structure (and also form a 3-dimensional quaternary structure whenever multiple subunits are involved) which only accept the shape of the active enantiomer. This is why only alpha-L-tocopherol has antioxidant activity, while its opposite, dextrorotary, enantiomer does not. When tocopherol or any other chiral substance is synthesized with common chemical reagents, the product is invariably a mixture of its 2 enantiomers, which is called racemic. Racemic mixtures cannot be separated into enantiomers because they have identical physical and chemical properties. The only ways to obtain pure, biologically active levorotary tocopherol are either to extract it from a biological source (organic) or to synthesize it using live enzymes in vitro reconstituting the tocopherol-anabolic pathway found in cats and other carnivores. All enzymes have poor shelf life and must be protected from excessive heat, freezing, detergents, and other denaturing agents, because destruction of tertiary and quaternary structures is irreversible and constitutes death of the enzyme. (Cooking is essentially denaturation of proteins, which is irreversible. Once an egg is scrambled, there is no way to unscramble it.)
Why are antioxidants so important? Because oxygen, which is essential to most modern life, is also toxic. All eukaryotic life forms require oxygen for the citric acid cycle, a.k.a. the Krebs cycle, and the electron transport chain of glucose catabolism, with oxygen being the ultimate electron acceptor (true to its nonmetallic nature), forming carbon dioxide and water. However, the catch to this catabolic energy bonanza is that when in aqueous solution, some of molecular oxygen (O2) rearranges into superoxide (O3-), until chemical equilibrium between molecular oxygen and superoxide is achieved. Superoxide is a free radical which is extremely corrosive, and generates multitudes of other free radicals that are equally caustic. This is why metals rust when wet or in humid climates. Guess what? Biologic structures such as neurons and arteries also rust out because of superoxide. This is why some bacteria, such as Porphyronas gingivalis, which causes gum disease, are obligate anaerobes, and are killed by the slightest exposure to oxygen. However, all eukaryotes (plants and phytoplankton, animals and zooplankton, and fungi) are blessed with organelles called peroxisomes in each and every cell, which are packed with antioxidants, the most common of which being superoxide dismutase (SOD). These enzymes are charged with neutralizing deadly (just ask P. gingivalis) superoxide and other free radicals it engenders. Peroxisomes make life in the modern oxidizing atmosphere possible (the early Earth had a reducing atmosphere; it only became an oxidizing atmosphere as a result of all the molecular oxygen produced by photosynthesis in plants). Kitties, as mentioned above, make their own vitamins C and E, but humans must take these in the diet.
The rusty arteries alluded to above account for another symptom of “metabolic disorder”: elevated cholesterol. An obvious metaphor for arteries is roads and highways. When these become potholed from harsh winters, barriers must be erected around them so that repairs can commence. This formation of road barriers is the purpose of the appallingly demonized low-density lipoproteins (LDL), so that the corrosion can be repaired by the high-density lipoproteins (HDL). Neither form of lipoprotein is “good” or “bad”; both are necessary and indispensible for the body to affectthe necessary repairs to its arteries. This is why cholesterol does not cause heart disease, and why statins (anti-cholesterol drugs) do not prevent heart attacks. Rather, neuronal membranes depend on having the waxy cholesterol amid its hydrocarbons to remain flexible; this is why statins cause Alzheimer. Any appearance that such drugs do help cardiovascular disease is the result of the widespread data falsification and misrepresentation endemic to the gross conflict of interest engendered by capitalism. It is impossible to do real science under capitalism! John Abramson, M.D. describes this fraud and chicanery in excruciating detail in his Overdo$ed America. This is one reason why I am a staunch socialist, and why socialism is a biblical mandate.